TRPM7 is required for ovarian cancer cell growth, migration and invasion

Wang, Jing; Liao, Qianjin; Zhang, Yi; Zhou, Hui; Luo, Chenhui; Tang, Jie; Wang, Ying; Tang, Yan; Zhao, Min; Zhao, Xueheng; Zhang, Qiong-yu; Xiao, Ling

doi:10.1016/j.bbrc.2014.10.118

Cited by 54 publications

(52 citation statements)

References 26 publications

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“…In some cases, splicing genes were themselves differentially spliced. For example, a long transcript variant of Rbfox2 (NM_053104) was up-regulated in Wnt-5a-4T1 cells while the short variant (NM_001110830) was down-regulated [37]. In the case of EOC, ESRP1 expression plays a role in EMT-related mechanisms since there were differences in the expression of EMT markers in ESRP1 down-regulated EMT cells.…”

Section: Discussionmentioning

confidence: 99%

Snail Driving Alternative Splicing of CD44 by ESRP1 Enhances Invasion and Migration in Epithelial Ovarian Cancer

Chen

Yao

Sun

et al. 2017

Cell Physiol Biochem

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Background/Aims: Our study aims to investigate the role, effect and mechanisms of ESRP1 (epithelial splicing regulatory protein 1) in epithelial-mesenchymal transition (EMT) in epithelial ovarian cancer (EOC). Methods: Microarray and immunohistochemical analysis of ESRP1 expression were performed in EOC cases. The correlations between ESRP1 expression and clinical factors on EOC were assessed. Lentivirus-mediated RNA interference and EGFP vector which contains ESRP1 gene were used to down-regulate and up-regulate ESRP1 expression in human EOC cell lines. Roles of ESRP1 in cell growth, migration and invasion of EOC cells were also measured by Cell Counting Kit-8 and Transwell systems in vitro and by a nude mice intraperitoneal transplantation model in vivo. Results: By the analysis of Gene Expression Omnibus (GEO) (p<0.05) and our own microarray data (p<0.001), ESRP1 expression in EOC was significantly different from normal ovarian tissue. It was abundant in the nuclei of cancer cells and in malignant lesions. However, it was weakly expressed or negative in both normal and benign lesions. High ESRP1 expression in EOC was associated with poor clinical outcomes. Decreased ESRP1 expression significantly increased cell migration and invasion both in vivo and in vitro. Snail strongly repressed ESRP1 transcription through binding to the ESRP1 promoter in EOC cells. Furthermore, ESRP1 regulated the expression of CD44s. Down-regulated ESRP1 resulted in an isoform switching from CD44v to CD44s, which modulated epithelial-mesenchymal transition (EMT) program in EOC. Up-regulatin of ESRP1 was detected in mesenchymal to epithelial transition (MET) in vivo. Conclusions: ESRP1 regulates CD44 alternative splicing during the EMT process which plays an important role in EOC carcinogenesis. In addition, ESRP1 is associated with disease prognosis in EOC.Jie Tang, MD, Ph.D, Professor 283 Tongzipo Road, Yuelu District,

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Section: Discussionmentioning

confidence: 99%

Snail Driving Alternative Splicing of CD44 by ESRP1 Enhances Invasion and Migration in Epithelial Ovarian Cancer

Chen

Yao

Sun

et al. 2017

Cell Physiol Biochem

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“…Migration and metastasis of cancer cells have been shown to depend also on Ca 2ϩ influx through several Ca 2ϩ -permeable TRP family members. Among them canonical TRPC1 (46,105) and TRPC6 (85), Mg 2ϩ -and stretch-regulated channel with kinase domain, TRPM7 (333,517,552), cold/ menthol-sensitive TRPM8 (368,536,553), and heat-activated TRPV2 (164,311,340,341,375). However, a number of questions regarding the mechanism(s) of their involvement still remain unanswered.…”

Section: Oncogenic Alterations In Ca 2ϩ Signalingmentioning

confidence: 99%

Ion Channels in Cancer: Are Cancer Hallmarks Oncochannelopathies?

Prevarskaya

Skryma

Shuba³

2018

Physiological Reviews

341

292

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Genomic instability is a primary cause and fundamental feature of human cancer. However, all cancer cell genotypes generally translate into several common pathophysiological features, often referred to as cancer hallmarks. Although nowadays the catalog of cancer hallmarks is quite broad, the most common and obvious of them are 1) uncontrolled proliferation, 2) resistance to programmed cell death (apoptosis), 3) tissue invasion and metastasis, and 4) sustained angiogenesis. Among the genes affected by cancer, those encoding ion channels are present. Membrane proteins responsible for signaling within cell and among cells, for coupling of extracellular events with intracellular responses, and for maintaining intracellular ionic homeostasis ion channels contribute to various extents to pathophysiological features of each cancer hallmark. Moreover, tight association of these hallmarks with ion channel dysfunction gives a good reason to classify them as special type of channelopathies, namely oncochannelopathies. Although the relation of cancer hallmarks to ion channel dysfunction differs from classical definition of channelopathies, as disease states causally linked with inherited mutations of ion channel genes that alter channel's biophysical properties, in a broader context of the disease state, to which pathogenesis ion channels essentially contribute, such classification seems absolutely appropriate. In this review the authors provide arguments to substantiate such point of view.

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“…In ovarian cancer (72) and bladder cancer, TRPM7 regulates cancer cell migration (60). TRPM7 also regulates proliferation of cancer cells (73)(74)(75), although silencing of TRPM7 does not affect the viability of breast cancer cells (61).…”

Section: Trp Channels In Cancer Metastasismentioning

confidence: 99%

Emerging role of transient receptor potential (TRP) channels in cancer progression

Yang

Kim

2020

BMB Rep.

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Transient receptor potential (TRP) channels comprise a diverse family of ion channels, the majority of which are calcium permeable and show sophisticated regulatory patterns in response to various environmental cues. Early studies led to the recognition of TRP channels as environmental and chemical sensors. Later studies revealed that TRP channels mediated the regulation of intracellular calcium. Mutations in TRP channel genes result in abnormal regulation of TRP channel function or expression, and interfere with normal spatial and temporal patterns of intracellular local Ca 2+ distribution. The resulting dysregulation of multiple downstream effectors, depending on Ca 2+ homeostasis, is associated with hallmarks of cancer pathophysiology, including enhanced proliferation, survival and invasion of cancer cells. These findings indicate that TRP channels affect multiple events that control cellular fate and play a key role in cancer progression. This review discusses the accumulating evidence supporting the role of TRP channels in tumorigenesis, with emphasis on prostate cancer. [BMB Reports 2020; 53(3): 125-132]

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TRPM7 is required for ovarian cancer cell growth, migration and invasion

Cited by 54 publications

References 26 publications

Snail Driving Alternative Splicing of CD44 by ESRP1 Enhances Invasion and Migration in Epithelial Ovarian Cancer

Snail Driving Alternative Splicing of CD44 by ESRP1 Enhances Invasion and Migration in Epithelial Ovarian Cancer

Ion Channels in Cancer: Are Cancer Hallmarks Oncochannelopathies?

Emerging role of transient receptor potential (TRP) channels in cancer progression

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